The CAV virus that has not been classified so far causes infectious anaemia in chicken. The virus was first isolated in Japan in 1979 and was given its name because of the serious anaemia caused by it in young chicks (Yuasa et al, 1979). The other symptoms of CAV infection are the atrophy of the bone marrow and destruction of lymphocytes in the thymus. Lesions occur in the spleen and liver.
Day-old chicks are most susceptible. In these animals lethargy, anorexia and a passing aneamia are observed from 4 to 7 days after inoculation with CAV and about half of the animals die between 2 and 3 weeks after infection. With increasing age the natural resistance also increases. Upon infection at the age of seven days the chicks only develop a passing anaemia after infection, and upon infection of 14 days old animals no anaemia follows.
Protection against CAV infection and CAV disease symptoms is highly based on humoral immunological defence mechanisms. Vielitz (1989) developed a practical, rather effective method of prevention by means of a "controlled exposure" with CAV-infected liver suspensions in layers, the offspring thus acquiring maternal immunity. In Germany this method of immunization is used in practice, but it does not seem to be quite risk-free.
Animal experiments conducted in isolated poultry houses with the Centraal Diergeneeskundig Instituut (CDI) at Letystad have confirmed the protective value of maternal antibodies. Here the "controlled exposure" was carried out with CAV multiplied in tissue culture. The presence of maternal antibodies against CAV fully prevented the CAV replication upon infection of day-old chicks from thus vaccinated mother animals. The CAV symptoms did not occur either. This passive protection was also obtained in offspring of immunized layers and also after injection of specifically pathogen-free (SPF) chicks with yolk extracts of eggs of the same immunized layers. The passive protection with respect to CAV infection by means of administration of CAV antibodies lasted until the age of 4 weeks. Then the passive protection was found to be incomplete. These experiments showed that maternal antibodies produced by vaccination of mother animals will play an important preventive role in the practical situation.
It has also been demonstrated by way of experiment that in chicks that survive the CAV infection a passing depletion of a specific population of thymus lymphocytes occurs (Jeurissen et al, 1989). The thymus atrophy is the possible cause of the immunodepression causing CAV, resulting in that specific vaccinations are less effective, e.g. against Newcastle Disease. CAV has been isolated several times in flocks with increased losses owing to Marek's disease, Gumboro's disease (Infectious Bursal Disease Virus, IBDV; Yuasa et al, 1980) and in animals with Blue Wing Disease in association with reoviruses (Engstrom, 1988a, Engstrom et al, 1988b). With experimental double infections the enhancing properties of CAV with respect to other chicken viruses (e.g. Marek's Disease Virus, MDV, De Boer et al, 1989a) have been demonstrated. Recently a sharply increased inoculation reaction was observed in our own experiments after aerosol vaccination with Newcastle Disease vaccine and simultaneous CAV infection. CAV therefore leads to immunosuppressive and enhancing effects on other virus infections. These properties of CAV probably cause an increased incidence of virulent disease outbreaks in practice.
CAV seems to be spread all over the world. A considerable time after the CAV research had started in Japan the first CAV isolations were conducted in Europe, namely in Germany by Von Bulow (1983) and later by McNulty et al (1990) in the United Kingdom. In the Netherlands the first isolations of CAV from material from the USA, Israel and Tunesia were conducted by De Boer et al (1988). The available literature data indicate that the isolates belong to one serotype but several field isolates are to be tested for their mutual relationship and possible differences in pathogenicity (McNulty et al, 1990). The spread of CAV within a flock probably occurs by infection via feces and air. Vertical transmission of virus to the offspring, however, also plays an important role in CAV epidemiology. In various countries the presence of CAV was demonstrated seriologically.
Under tissue culture conditions CAV is hard to multiply. CAV hitherto causes only a cytopathologic effect (CPE) in MDV transformed lymphoblastoid cell lines from lymphomas of Marek's disease (MDCC-MSB1 cells) or Avian Leukaemia Virus (ALV) transformed lymphoblastoid cell lines from lymphold leukosis (1104-X5 cells; Yuasa, 1983).
A recent study by Todd et al (1990) describes virus particles (in purified CAV material) having a diameter of 23.5 nm which concentrate at a density of 1.33-1.34 g/ml in a CsCl gradient. The virus has one predominant polypeptide (Mr: 50,000) and a circular single-stranded DNA genome having a length of 2.3 kilobases. Two small viruses, the Porcine Circovirus and a virus associated with Psittacine Beak and Feather Disease, resemble CAV as regards the circular single-stranded DNA but have a smaller genome and a smaller virus particle diameter (Ritchie et al, 1989; Tischer etal, 1982). It was accepted for a long time that CAV belonged to the parvoviruses. Although most of the parvoviruses are single-stranded DNA viruses, they possess linear DNA, a larger genome and probably also another composition of viral polypeptides.